JAC Advance Access published online on September 4, 2008
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkn375
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Original research |
Staphylococcus hominis subsp. novobiosepticus strains causing nosocomial bloodstream infection in Brazil
1 Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Av. dos Bandeirantes 3900, Brazil 2 Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Via do café, s/n°, Monte Alegre, Ribeirão Preto, SP CEP 14040-903, Brazil 3 Fundação Faculdade de Ciências Médicas de Porto Alegre, R. Sarmento Leite, 245, Porto Alegre, RS CEP 90050-170, Brazil 4 Laboratório Especial de Microbiologia Clínica, Universidade Federal de São Paulo, R. Botucatu, 740, São Paulo, SP CEP 04023-900, Brazil
Received 24 May 2008; returned 5 August 2008; revised 8 August 2008; accepted 11 August 2008
* Corresponding author. Tel: +55 16-36024290; Fax: +55 16-36024725; E-mail: aldarini{at}fcfrp.usp.br
Objectives: To report the isolation of six Staphylococcus hominis subsp. novobiosepticus (SHN) strains from hospitalized patients with bloodstream infections in two Brazilian hospitals and to characterize their susceptibility profile to several antimicrobials.
Methods: Species identification was performed by biochemical methods and sodA gene sequencing. The MICs of antimicrobials were determined by broth and agar dilution methods and by Etest. Isolates were typed by PFGE and PCR amplification was used to detect the ccr gene complex and the mec class. Morphometric evaluation of cell wall was performed by transmission electron microscopy (TEM).
Results: Susceptibility profiles indicated that the majority of isolates (five) were multidrug-resistant. Overlapping and multiplex PCR showed that five out of the six strains harboured SCCmec type III with class A mec and type 3 ccr. The initial vancomycin MIC value of 4 mg/L for these strains increased to 16–32 mg/L after growth for 10 days in BHI broth supplemented with this antimicrobial. TEM indicated that vancomycin resistance was associated with cell wall thickening and to another mechanism not fully elucidated. Only one SHN strain was oxacillin- and vancomycin-susceptible. The nosocomial infections in at least five of the patients from both hospitals were caused by a single clone of SHN.
Conclusions: It is very important to consider SHN strains as the cause of nosocomial infections. The clinical implications resulting from the pattern of multidrug resistance in these strains may be complicated by the emergence of vancomycin resistance.
Key Words: staphylococci , mecA , vancomycin , mechanism of resistance